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Epidemiology

The exact incidence and prevalence are unknown. It is most commonly seen in amateur and professional sports players where head contact is common (e.g. boxing, American football, rugby, ice hockey), as well as in military personnel exposed to explosive blasts 1,3.

Clinical presentation

Symptoms have an insidious onset, most often years after the initial injuries, with loss of normal attention, concentration and memory. This can progress, in some cases in 2-3 years, to include motor symptoms such impaired gait, impaired, executive function, lack of insight and poor judgement 1,2,4.

Histology

Chronic traumatic encephalopathy is characterised by the presence of neurofibrillary tangles and TDP-43 binding protein in subcortical and perivascular regions, often with reactive astrocytes and microglia 7.

Pathophysiology

Although the details remain to be elucidated, there is mounting evidence that reactive gliosis and redistribution of aquaporin 4 molecules, leading to disruption of transparenchymal CSF clearance of interstitial beta-amyloid via the glymphatic system may be a key component 8.

Radiographic features

MRI

Imaging features of CTE are nonspecific but the following may be seen 4,7

Differential diagnosis

There is clinical and imaging overlap of chronic traumatic encephalopathy with other neurodegenerative diseases, and traumatic brain injury is a risk factor for their development (i.e. not just chronic traumatic encephalopathy) and should be considered in the differential diagnosis 5,6:

Related articles

Neurodegenerative diseases

Neurodegenerative diseases are legion and their classification just as protean. A useful approach is to divide them according to underlying pathological process, although even using this schema, there is much overlap and thus resulting confusion.